1. Field of the Invention
The present invention relates to devices for determining the optimal rate for emission of a stimulation pulse to a heart.
2. Description of the Prior Art
The ability to control the heart rate by means of electrical stimulation is important to the well-being and survival of many people afflicted by various defects in the function of their hearts. Battery-powered stimulation devices are available for different kinds of disorders.
The heart comprises a left atrium, right atrium, left ventricle and right ventricle and contains e.g. a sinus node (sinoatrial node. SA node), an area made up of special tissue in the wall of the heart's right atrium. In the normal, healthy state this area emits periodic, recurrent electrical pulses, each of which starting a heart cycle. When the pulse from the sinus node is propagated across the walls of the atrium, it triggers contraction of the atrium for expulsion of blood into the corresponding ventricle. The pulse is carried to another tissue area in the heart which has a special delay function, the atrioventricular (AV) node, from which it is carried on special electrically conductive tissue pathways to the ventricles. It is during this phase, when the electrical pulse passes along the conductive pathways to the ventricular walls, that blood is "pumped" from the atrium to ventricle. By the time this pulse arrives to trigger contraction of the ventricles, the ventricles have been expanded by inflowing blood and are ready to contract in order to pump blood to the lungs and circulatory system. After each contraction of the ventricles, a resting period starts during which the atria fill with blood, and lasts until the SA node generates the next pulse.
Normal rhythm, i.e. sinus rhythm, arises in the SA node. A faulty rhythm or rate, i.e. arrhythmia, can develop for different reasons. For example, the pathways, made of electrically conductive tissue, to or in a ventricle may be damaged or blocked so pulses emitted in the atrium are unable to trigger any contraction of the ventricle. In such cases, an electrical stimulation pulse can be supplied by an electronic stimulation device, i.e. a pacemaker. The generating of stimulation pulses by most of the stimulation devices currently in use is synchronized with or generally dependent on the heart's intrinsic electrical activity. This activity can be monitored with sensor electrodes placed somewhere in the patient's body, e.g. in or adjacent to the heart.
These sensor electrodes in an appropriate system sense electrical voltages generated during heart activity. The electrical voltage sensed with surface electrodes on the exterior of the body has the following general morphology during a heart cycle: A low voltage pulse, the P wave, designates an atrial event, corresponding to depolarization of muscle cells in the walls of the atria, causing these walls to contract. A more complex pulse segment is referred to as the QRS complex and encompasses e.g. a large electrical pulse. This area designates a ventricular event in the form of depolarization of muscle cells in ventricular walls when these cells contract, and the heart's actual blood-pumping process is started and performed. A low voltage pulse further designates the start of repolarization of the cells in ventricular walls, i.e. recovery from their preceding contraction, and is referred to as the T wave. These pulses/pulse segments normally follow each other over time, i.e. a P wave starts first in a heart cycle, followed by the QRS complex and, finally, the T wave. These segments are not always distinguishable in the electrical voltage sensed by sensor electrodes placed in or by the heart. Thus, no T wave and often not even the QRS complex are discernible with an electrode placed in an atrium. The P wave is not visible with an electrode in the ventricle.
A typical stimulation device can operate in the following general manner: The stimulation device awaits an atrial event, signaled by corresponding electrical activity in the heart, i.e. in practice the aforesaid P wave. If no P wave is detected within a first period of time (an atrial escape period), a stimulation pulse is sent to the atrium of the heart, stimulating muscle cells in atrial walls and causing them to contract. A ventricular event is then awaited, i.e. the device analyzes the voltage signal from the heart with respect to the presence of a QRS complex. If no such complex is detected within a second period of time (a ventricular escape interval), a stimulation pulse is sent to the ventricle, whereupon electrical activity in the atrium is again awaited. The interval between emission of stimulation pulses to the atrium and ventricle is equal to the difference in time between the first and second interval and is referred to as the AV delay. It normally corresponds to an interval lasting 100-200 milliseconds.
Normally, rate-modulating stimulation devices in current use determine the rate for emitting stimulation pulses as a function of the measurement value(s) for one or a plurality of parameters related to the physical load to which a person is subjected. These measurement values are sensed by suitable sensors devised in different ways. One such sensor can be an electrically powered flow meter, as shown in the published European patent application 0 634 192. In other instances, the impedance of a heart ventricle is determined and, accordingly, stroke volume. Electrical impedance is measured between a stimulation electrode in a ventricle and some other electrode in the body or, especially. the heart, as is the case in U.S. Pat. No. 5,417,715 which is included as a reference.
In certain embodiments, e.g. as described in the aforementioned U.S. patent, only the ongoing heart cycle is reviewed, and an appropriate time for the generating of a stimulation pulse is mainly determined from measurement values previously obtained in the same cycle, whereas measurements in previously proposed embodiments are made over a plurality of heart cycles which, in certain instances, may be well-separated in time. In principle, as is also discussed in the aforementioned U.S. patent, a well-selected or advantageous time for stimulating a heart is deemed to be when there is sufficient blood in a ventricle for it to be pumped out of same. Such a stimulation largely resembles the one which occurs naturally in a healthy heart. So an effort should be made to select a heart rate enabling these times to be achieved or at least times which are not too far removed from them. Heart stimulator designs supplying such times are previously known through e.g. the aforementioned U.S. patent and are discussed below.
The European patent EP-B1 0 551 355 shows how the interval elapsing between two consecutive stimulation pulses is continuously varied or reset with the aid of measurement of a parameter for the heart's activity. The parameter is measured as related to a single change in the duration of the stimulated heart cycle compared to the measurement value for the preceding heart cycle. The individual changes, only made for measurement purposes, are performed with intervals between them which do not affect general pressure in the circulatory system. The parameter is impedance between e.g. an electrode placed in the heart and a pacemaker housing, and this impedance represents, or is related to, the heart s stroke volume. The ratio is formed between impedance changes, with changes of equal but opposite magnitude, in the interval between stimulation pulses, and this value is compared to a reference value which can be constant or dependent on heart rate. When hemodynamic rate optimization is proposed, the time elapsing between two stimulation pulses is reduced on individual occasions until the change in impedance stops increasing. a procedure supplying a measure of the stroke volume. Here, it must be assumed that normal stimulation is too slow and utilizes a sub-optimal stimulation rate, which should be the result with a rate corresponding to the interval used when the change in impedance stops increasing.
U.S. Pat. No. 5,156,147 shows an adaptive pacemaker in which the change in the heart's pumped volume per unit of time, i.e. cardiac output (CO). is determined when heart rate increases. If the change is negative, i.e. reduced cardiac output then results, the increase in heart rate is canceled. It also notes that the increase in one possible embodiment can be also canceled if the increase in heart rate causes a drop in the increase rate for cardiac output.